The benign occipital epilepsies of childhood: an overview of the idiopathic syndromes and of the relationship to migraine.
ABSTRACT Benign occipital epilepsy of childhood is an idiopathic partial epilepsy syndrome with elementary visual symptomatology, frequently associated with other ictal phenomena. Seizures are usually followed by postictal headache and are often associated with interictal occipital rhythmic paroxysmal EEG activity that appears only after eye closure. In some children the ictal visual symptoms or the interictal EEG abnormalities may not be demonstrated. The clinical and/or EEG manifestations of other forms of idiopathic partial or generalized epilepsy may be found in association. Occipital spikes in non-epileptic children with defective vision, occipital slow spike-and-wave found in some patients with the Lennox-Gastaut syndrome, focal epilepsy due to occipital lesions, seizures originating in the temporal lobe secondary to an occipital abnormality, and complicated or basilar migraine must be considered in the differential diagnosis. Early-onset benign occipital epilepsy or seizure susceptibility syndrome deserves to be considered separately. It has been defined by Panayiotopoulos as consisting of brief, infrequent attacks or prolonged status epilepticus and characterized by ictal deviation of the eyes and/or head and vomiting, occurring in children usually between the ages of 3 and 7 years. Advances in molecular genetics will help decide whether these two disorders are indeed distinct. Benign occipital and benign rolandic epilepsy are commonly associated with migraine. The selective involvement of the occipital lobe in migraine has not been fully explained. The association between benign occipital epilepsy and migraine is likely related to this underlying mechanism as well. The "fixation off" phenomenon or blocking of occipital epileptic discharges by eye opening is not specific to benign occipital epilepsy of childhood and may be found in symptomatic epilepsies as well. Migraine and epilepsy are distinct disorders, both as far as their pathophysiologic mechanisms and clinical symptomatology are concerned. There is however an overlap in some patients and a causal relationship may exist in some, leading to clinically distinct migraine epilepsy syndromes. Here too, clarification of the molecular basis of migraine and of epilepsy will throw light on the nature of the relationship between the two conditions.
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- "Several epidemiological studies indicate that migraine and epilepsy may be strongly associated: the prevalence of migraine in patients with epilepsy ranged from 14 to 24%, and the prevalence of epilepsy in migraine subjects ranged from 1.1 to 17%   . An association with migraine has been reported in specific epileptic syndromes, including benign occipital epilepsy of childhood and benign rolandic epilepsy  . Comorbidity of epilepsy included migraine in a national survey done in Canada  . "
ABSTRACT: The prevalence and characteristics of interictal headache, epilepsy and headache/epilepsy comorbidity were assessed in 858 women and 309 men aged 18-81 years from headache and epilepsy centers in Italy. The research hypothesis was that comorbidity among patients with either disorder would be expected to be higher than in the general population. Interictal headache was diagnosed in 675 cases (migraine 482; tension-type headache 168; other types 25), epilepsy in 336 (partial 171; generalized 165) and comorbidity in 156 (1.6% from headache centers; 30.0% from epilepsy centers). Patients with epilepsy, headache and comorbidity differed in a number of demographic and clinical aspects. However, for both headache and epilepsy, a family history of the same clinical condition was equally prevalent in patients with and without comorbidity. These findings do not support the purported association between headache and epilepsy.Epilepsy & Behavior 02/2012; 23(3):342-7. DOI:10.1016/j.yebeh.2012.01.017 · 2.06 Impact Factor
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- "Although not fully elucidated, a relationship between migraine and epilepsy has long been postulated, with clinical and epidemiological studies demonstrating that both entities are highly comorbid            . As both these disorders are characterized by transient paroxysmal episodes of altered brain function, one condition may be mistaken for the other            . Epilepsy and migraine may either coexist independently in the same individual or be associated by chance; the outcome of this comorbidity is that one of these disorders may lead to, or mimic, the other. "
ABSTRACT: The few reports that have been published on the current International Classification of Headache Disorders, Second Edition (ICHD-II), criteria for migralepsy and hemicrania epileptica have highlighted the considerable confusion regarding this "hot topic" within both headache and epilepsy classifications (ICHD-II and International League Against Epilepsy [ILAE]). Indeed, the ICHD-II describes a migraine-triggered seizure as a rare event in which a seizure occurs during migraine aura; on the other hand, hemicrania epileptica is described as an "ictal headache" that occurs "synchronously" with a partial seizure. To confuse matters even further, neither the term migralepsy nor the term hemicrania epileptica is included in the currently used ILAE classification. On the basis of both a review of "migralepsy" cases in the literature and 16 additional retrospective multicenter cases, we suggest that the term migraine-triggered seizure or migralepsy be deleted from the ICHD-II classification until unequivocal evidence is provided of its existence, and that the term ictal epileptic headache be introduced into the ILAE classification.Epilepsy & Behavior 05/2011; 21(1):52-9. DOI:10.1016/j.yebeh.2011.03.004 · 2.06 Impact Factor
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- "Reciprocal comorbidity between epilepsy and migraine, two common childhood conditions, has long been recognized (Froelich et al., 1960; Lennox & Lennox, 1960), and the association with migraine has been shown to apply across idiopathic, cryptogenic, and symptomatic classes of epilepsies (Ottman & Lipton, 1994). Among idiopathic epilepsies, benign occipital epilepsy has the strongest association with migraine (Andermann & Zifkin, 1998). Surprisingly, however, evidence of migraine comorbidity with rolandic epilepsy (RE), the more common idiopathic partial epilepsy, is conflicting (Santucci et al., 1985; Bladin, 1987; Giroud et al., 1989; Septien et al., 1991; Andermann & Andermann , 1992; Wirrell & Hamiwka, 2006). "
ABSTRACT: Evidence for a specific association between migraine and rolandic epilepsy (RE) has been conflicting. Children with migraine frequently have electroencephalographic (EEG) abnormalities, including rolandic discharges, and approximately 50% of siblings of patients with RE exhibit rolandic discharges. We assessed migraine risk in RE probands and their siblings. We used cohort and reconstructed cohort designs to respectively assess the relative risk of migraine in 72 children with RE and their 88 siblings using International Classification of Headache Disorders (ICHD-2) criteria. Incidences were compared in 150 age and geographically matched nonepilepsy probands and their 188 siblings. We used a Cox proportional hazards model, using age as the time base, adjusting hazard ratios (HRs) for sex in the proband analysis, and for sex and proband migraine status in the sibling analysis. Prevalence of migraine in RE probands was 15% versus 7% in nonepilepsy probands, and in siblings of RE probands prevalence was 14% versus 4% in nonepilepsy siblings. The sex-adjusted HR of migraine for an RE proband was 2.46 [95% confidence interval (CI) 1.06-5.70]. The adjusted HR of having > or =1 sibling with migraine in an RE family was 3.35 (95% CI 1.20-9.33), whereas the HR of any one sibling of a RE proband was 2.86 (95% CI 1.10-7.43). Migraine is strongly comorbid in RE and independently clusters in their siblings. These results suggest shared susceptibility to migraine and RE that is not directly mediated by epileptic seizures. Susceptibility gene variants for RE may be tested as risk factors for migraine.Epilepsia 09/2009; 50(11):2428-33. DOI:10.1111/j.1528-1167.2009.02240.x · 4.58 Impact Factor